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PubMed2005

Occupational and environmental factors and idiopathic pulmonary fibrosis in Japan.

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing interstitial lung disease of unknown etiology. Environmental factors, especially occupational agents, may be of great importance in the manifestation of IPF. We examined the relationship between occupational and environmental factors and IPF in Japan. A multicenter hospital-based case-control study was performed in 2001. Included were 102 cases aged 40 years or over who were within 2 years of having been diagnosed in accordance with the most recent criteria. Controls, aged 40 years or over, were 55 hospitalized patients diagnosed as having acute bacterial pneumonia and four outpatients with common colds. Data on occupational and environmental factors were obtained from a questionnaire. Multiple logistic regression analysis was used to estimate the adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of IPF for single factors with adjustment for age, sex and region. Compared with controls, cases were more likely to have been managers, officials or production workers and less likely to have been protective service or materials handling workers. Clerical and related work was significantly related to a decreased risk of IPF after further adjustment for pack-years of smoking (OR = 0.42; 95% CI = 0.18-0.95). Exposure to metal dust was significantly associated with an increased risk of IPF (OR = 9.55; 95% CI = 1.68-181.12). From 20.0 to 39.9 pack-years of smoking was significantly associated with an increased risk of IPF (OR = 3.23; 95% CI = 1.01-10.84). Our results appear to confirm data from previous epidemiologic studies. Metal dust exposure may be a particularly important risk factor for IPF.

Adult↗
PubMed2005

Expression of apoptotic and antiapoptotic markers in epithelial cells in idiopathic pulmonary fibrosis.

STUDY OBJECTIVE: Idiopathic pulmonary fibrosis (IPF) is a chronic, usually fatal lung disease of unknown etiology. A common feature is the presence of microscopic areas of epithelial cell dropout. Increased apoptosis of these cells could elucidate the speculative pathogenesis of the disease. Therefore, the aim of our study was to examine the expression of p53, p21, bcl-2, bax, and caspase-3 in association with DNA strand breaks in bronchial and alveolar epithelial cells in lung specimens from IPF patients and control subjects. PATIENTS AND METHODS: We examined by immunohistochemistry the expression of p53, p21, bax, bcl-2, and caspase-3 in association with DNA strand breaks detected by terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) in bronchial and alveolar epithelial cells in lung specimens taken by biopsy in 12 IPF patients and 10 control subjects. An independent tissue evaluation by two pathologists graded semiquantatively the degree of staining present. RESULTS: TUNEL was positive in epithelial cells in all IPF patients and only in one control subject. The expression of p53, p21, bax, and caspase-3 was up-regulated in IPF patients compared to control subjects. Bcl-2 was expressed less in IPF patients than in control subjects. CONCLUSIONS: These results confirm that apoptotic hyperplastic epithelial cells are present in patients with IPF and that the expression of p53, p21, bax, and caspase-3 appears to be up-regulated and that of bcl-2 down-regulated in these cells. The increased expression of proapoptotic molecules in epithelial cells in IPF may be involved in the inadequate and delayed reepithelialization, which in turn contributes to fibroblast proliferation.

Apoptosis↗
PubMed1999

Interstitial lung disease clinics for the management of idiopathic pulmonary fibrosis: a potential advantage to patients. Greater Manchester Lung Fibrosis Consortium.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) has a relatively poor prognosis with limited therapeutic intervention. This has led to varying practices, from a nihilistic approach at one end to more aggressive management at the other. However, a dedicated clinic with a multidisciplinary approach may offer advantages to patients with IPF. METHODS: A retrospective observational study was performed to compare patients with a diagnosis of IPF attending a general respiratory clinic between January 1988 and December 1996 to those attending a interstitial lung disease (ILD) clinic between January 1992 and December 1996. The notes were reviewed for (1) confirmation of diagnosis, (2) method of diagnosis, (3) date of initial consultation, and (4) survival. The end point was death, and the number of deaths that occurred up to October 1997 was recorded. RESULTS: The study identified 148 patients with a diagnosis of IPF. Ten patients underwent transplantation and were excluded. Of the remaining 138, 84 patients attended the general respiratory clinic (mean age 65 years: 53 men [63%], 31 women), and 54 attended the ILD clinic (mean age 56 years: 26 men [48%], 28 women). Patients attending the ILD clinic had a median survival of >3714 days. Patients attending the general respiratory clinic had a median survival of 1796 +/- standard error 437 days (CI 940-2652), p = .032 Breslow. Age was an important determinant of outcome. For patients less than 60 years of age (n = 60), the median survival for the ILD clinic was >3700 days, compared to 2535 +/- 577 days (CI 1404-280) in the general respiratory clinic, p = .037 Breslow. There was no difference in survival of patients over 60 years of age. CONCLUSIONS: The study suggests that a dedicated multidisciplinary clinic may result in an improved outcome for patients with IPF, particularly for patients younger than 60 years. This has implications that may facilitate the development of suitably powered therapeutic trials and may affect patient referral for transplantation.

Ambulatory Care Facilities↗
PubMed1999

[An experimental study on the effect of azithromycin treatment in bleomycin-induced pulmonary fibrosis of rats].

OBJECTIVE: To evaluate the therapeutic effects and mechanism of azithromycin treatment in bleomycin-induced pulmonary fibrosis of rats. METHODS: Animal model of bleomycin-A5-induced pulmonary fibrosis was established in rats.36 animal models were divided into two groups: a bleomycin-induced pulmonary fibrosis group and a azithromycin group in which the animal models were treated with azithromycin (80 mg/kg once a day for three continuous days in a week). The animals of the two groups were killed at the first,second and fourth week respectively. Another six rats constituted a normal control group, instillated withsaline intratracheally and killed at the first week. Pathological changes activity of nuclear factor kappaB (NF-kappaB) of alveolar macrophage, cytokine tumor necrosis factor (TNF) alpha, transforming growth factor-beta (TGF-beta) mRNA expression and protein levels of alveolar macrophage and lung tissue were studied or measured. RESULTS: Amelioration of alveolitis and lung fibrosis after treatment with azithromycin was shown in pathological section (P < 0.05). The activity of NF-kappaB was significantly higher in one-week pulmonary fibrosis model than that in normal control and its level in alveolar macrophage reduced (67.2%) after treatment with azithromycin. The level of protein and mRNA of TNFalpha, TGF-beta in lung tissue and alveolar macrophage was increased in the early stage of pulmonary fibrosis and reduced after treatment with azithromycin (P < 0.05). CONCLUSION: It is suggested that azithromycin might be a therapeutic drug for pulmonary fibrosis in the future. Azithromycin reduced the degree of alveolitis and fibrosis through inhibition of the activity of NF-kappaB and the expression of TNFalpha, TGF-beta mRNA and lowering the level of protein in alveolar macrophage and lung tissue in the early stage of pulmonary fibrosis. This might be one of the mechanisms of azithromycin treatment in pulmonary fibrosis.

Animals↗
PubMed2000

Circulating bronchoepithelial cells expressing mRNA for surfactant protein A in patients with pulmonary fibrosis.

There are several unsolved clinical findings in patients with idiopathic pulmonary fibrosis (IPF); (i) predominance of fibrosis in the lower lung fields, (ii) digital clubbing, and (iii) patchy distribution of pulmonary fibrosis. To explain these unsolved problems, we hypothesized that regenerated or premature bronchoepithelial cells may circulate in the blood in patients with IPF. To prove this, we performed the reverse transcriptase-polymerase chain reaction (RT-PCR) for cytokeratin 19 (CK19) and pulmonary surfactant protein A (SPA) in peripheral blood in patients with IPF and pulmonary fibrosis associated with collagen vascular disorders. In addition, 20 patients with chronic pulmonary emphysema as a disease control and 19 normal volunteers were also evaluated for the existence of circulating bronchoepithelial cells. RT-PCR analysis showed that CK19 was expressed in 12 of 38 blood samples (31.6%) of IPF and pulmonary fibrosis associated with collagen vascular disorders, seven of 20 (35.0%) blood samples of chronic pulmonary emphysema, and four of 19 (21.1%) blood samples of normal volunteers. mRNA for SPA was positive in eight of 38 (21.1%) blood samples of IPF. In contrast, SPA expressing cells were not detected in any blood samples obtained from patients with chronic pulmonary emphysema or normal volunteers. This evidence suggests that there were some circulating bronchoepithelial cells expressing mRNA for SPA in peripheral blood of patients with IPF and pulmonary fibrosis associated with collagen vascular disorders.

Adult↗
PubMed1995

Pulmonary fibrosis correlates with outcome in adult respiratory distress syndrome. A study in mechanically ventilated patients.

STUDY OBJECTIVE: The present study was carried out to evaluate the prognostic value of pulmonary fibrosis diagnosed on the basis of pulmonary samples obtained by fiberscopic transbronchial lung biopsy (TBLB) in patients treated for severe established adult respiratory distress syndrome (ARDS). DESIGN: Prospective cohort study. SETTING: Intensive Care Unit of a University Hospital. PATIENTS: Consecutive patients with a diagnosis of established ARDS. INTERVENTIONS: Samples of pulmonary tissue (3 to 6 in each patient) were obtained by fiberoptic TBLB. Severity of pulmonary fibrosis was assessed based on pathologic changes. Hematoxylin and eosin and Masson's trichrome stains were performed on each tissue sample. MAIN RESULTS: Twenty-two lung specimens were obtained from 25 consecutive patients with ARDS of various origin (postsurgical complications, 7 patients; multiple trauma, 8 patients; medical problems, 7 patients). Transbronchial lung biopsy was complicated by small or moderate hemorrhage in three patients. No case of pneumothorax was identified. Pathologic findings showed that 14 patients (64%) had pulmonary fibrosis, either mild (9 patients) or moderate to severe fibrosis (5 patients). In the patients with pulmonary fibrosis, mortality rate was 57% (8 out of 14 patients), which was significantly different (p < 0.02) from the 0% mortality rate observed in patients without pulmonary fibrosis. Severity of pulmonary fibrosis (mild vs moderate and severe) did not influence outcome. With the exception of pathologic findings, characteristics of patients with and without pulmonary fibrosis (PaO2, PaCO2, the ratio of PaO2 to fraction of inspired oxygen, and positive end-expiratory pressure) were not different. CONCLUSION: In the study patients, pulmonary fibrosis diagnosed on the basis of TBLB was closely related to fatality in established ARDS.

Adult↗
PubMed2006

[Kinetics and mechanism in bleomycin-induced murine pulmonary fibrosis model].

OBJECTIVE: To investigate the kinetics of pathogenesis of bleomycin induced pulmonary fibrosis and its mechanism in mice. METHODS: Thirty six male ICR mice were randomized as a negative control (NC) group and pulmonary fibrosis model (FM) groups (FMA, FMB, FMC, FMD, FME sub groups). Except for NC group, mice in the other groups were given bleomycin by nasal instillation. Animals in each group were sacrificed on day 6, 14, 21, 28 and 35, respectively. T lymphocytes were quantified for Th1/Th2 and Tc1/Tc2 by flow cytometry. Accumulation of inflammatory cells in bronchioalveolar lavage fluid (BALF) was quantified by cell count. The sections of the right lung were stained with either hematoxylin eosin (HE) or Masson trichrome. The left lung was weighed and its hydroxyproline (HYP) content was assayed. Multi cytokine expression in lung tissue was assayed by semi quantitative reverse transcription polymerase chain reaction (RT-PCR). On day 35, the tidal volume (V(T)), forced expiratory volume in 1 second/forced vital capacity (FEV 0.1/FVC), static compliance (Cst) of mice were determined before they were sacrificed. RESULTS: (1)The total cell number in BALF in pulmonary fibrosis groups was statistically significantly higher than that in NC group (all P<0.01), and HYP content in lung tissue in pulmonary fibrosis groups was statistically significantly increased than that in NC group except for group FMA (all P<0.01). (2)V(T) and Cst in FME group were statistically significantly decreased than those in NC group (both P<0.01), and FEV 0.1/FVC was statistically significantly increased (P<0.05). (3)Th1 and Tc1 were demonstrated as the dominant expression in the acute inflammatory stage; Th2 and Tc2 were the dominant expression in the fibrosis forming stage, and then Th1 and Tc1 were again the dominant expression at the terminal stage of pulmonary fibrosis. (4)Compared with the content of cytokine in the lung in NC group, the expression of transforming growth factor-beta1 (TGF-beta1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA were significantly higher in FM groups (all P<0.01). CONCLUSION: The changes in lung function of bleomycin-induced pulmonary fibrosis in mice are typical of that of restrictive ventilatory disorder. Th2, Tc2 and fibrotic promoting growth factors (TGF-beta1, TIMP-1, etc.) play pivotal roles in the pathogenesis of pulmonary fibrotic process.

Animals↗
PubMed1984

Effect of oxygen concentration on pulmonary fibrosis caused by peplomycin in mice.

The pulmonary fibrosis caused by peplomycin (PEP) was studied in terms of oxygen toxicity using ICR mice. When 16 micrograms of PEP was administered intratracheally in mice after exposure to the air containing 75% O2 for 10 days, the pulmonary fibrosis was completely suppressed, while when mice were exposed to 75% O2 after the administration of PEP, the fibrosis was much severe than that of mice raised in atmospheric air. In 50% O2, similar oxygen effect was also observed, but it was weaker than that in 75% O2. In 90% O2, the oxygen toxicity was observed in mice without administration of PEP. When mice were exposed to 75% O2, the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, which are relevant to the detoxication of active oxygen species, were not increased in the lung, but the levels of reducing agents such as glutathione and ascorbic acid, and high molecular substances having 1O2-scavenging activity were enhanced. The results suggest that these materials have some roles to decrease the pulmonary fibrosis caused by PEP.

Animals↗
PubMed2002

Idiopathic pulmonary fibrosis: current and future treatment options.

Idiopathic pulmonary fibrosis (IPF) is a chronic condition of unknown etiology with an unfavorable outcome from progressively deteriorating respiratory function, leading ultimately to death from respiratory failure. It is characterized by sequential acute lung injury resulting in progressive fixed tissue fibrosis, architectural distortion and loss of function. An excess of profibrotic cytokines and/or a deficiency in antifibrotic cytokines have been implicated in the pathological process as has excessive oxidation. IPF is distinguished from other forms of diffuse pulmonary fibrosis by the presence of the specific histological pattern of usual interstitial pneumonitis. Oral corticosteroids are the usual treatment, but objective response rates are poor and good quality studies do not exist. Other therapies either alone or in combination with corticosteroids are widely used, including azathioprine, colchicine, cyclophosphamide and penicillamine. There is a paucity of good quality information regarding the effectiveness of most noncorticosteroid immunosuppressive agents. Older studies of lesser methodological quality have shown benefits from these drugs, generally when added to corticosteroids. Many were retrospective reviews or uncontrolled, nonrandomized, open-label, prospective studies and often included other histological patterns of disease which are now thought to respond better to immunosuppressive agents. The results of intervention with colchicine and azathioprine have been disappointing when assessed by good quality trials using modern diagnostic criteria. Modern high quality studies are lacking for several agents, notably cyclophosphamide and penicillamine. The older agents may yet prove to be effective but further good quality trials will be necessary to assess these agents adequately. Other new anti-inflammatory, antioxidant, antifibrotic or anticytokine compounds are largely untried or unreported. One trial using interferon-gamma-1b showed a significant improvement in pulmonary function but there are concerns regarding the generalizability of this study. Pirfenidone, cyclosporine and acetylcysteine may also prove to be of benefit but current studies are of insufficient quality to allow for any conclusions to be drawn. Currently there is no good evidence to support the routine use of oral corticosteroids, azathioprine, cyclophosphamide, penicillamine, colchicine, cyclosporine or any other immunosuppressive, antifibrotic or immunomodulatory agent in the management of IPF. Interferon, pirfenidone and other new agents may be of benefit but further studies are required. Any recommendations for treatment must therefore be made on an individual and empiric basis. As some other forms of pulmonary fibrosis may respond better to immunosuppressive agents, it remains important to make an accurate diagnosis, by open lung biopsy if necessary.

Adjuvants, Immunologic↗
PubMed1998

Algorithm for diagnosing pulmonary fibrosis in tropical countries.

An algorithm for diagnosis of pulmonary fibrosis in the tropical countries has been developed on the basis of the common causes of fibrosis, and the availability and feasibility of different diagnostic techniques in those countries. First, it is important to exclude common diseases such as the atypical or occult forms of bronchiectasis, pulmonary tuberculosis, and chronic bronchitis, which often overshadow interstitial pulmonary fibrosis. A good history and physical examination supplemented with chest radiography and simple lung function tests are generally enough to narrow down the list of causes of diffuse lung disease to interstitial pulmonary fibrosis. The real difficulty lies in identifying the idiopathic or "lone" forms from the secondary forms of pulmonary fibrosis. High-resolution CT is helpful in a large number of patients. Transbronchial lung biopsy is performed in a select population of patients. Open surgical or thoracoscopy guided biopsy is the gold standard, but is rarely required.

Algorithms↗
PubMed1968

Carcinoma of the lung and diffuse interstitial pulmonary fibrosis.

The clinical and histopathological findings are presented in two cases of diffuse interstitial pulmonary fibrosis in which carcinoma of the lung developed. In one case with rheumatoid arthritis and diffuse interstitial pulmonary fibrosis there was ;malignant pulmonary adenomatosis', an association which does not appear to have been reported before. In the second case idiopathic diffuse interstitial pulmonary fibrosis was complicated by large cell anaplastic carcinoma of the lung. It is suggested that in both cases the development of carcinoma of the lung was a complication of the epithelial hyperplasia and scarring that occurs in diffuse interstitial pulmonary fibrosis. It is also suggested that carcinoma found in the main bronchi in patients with diffuse interstitial pulmonary fibrosis should not be regarded as coincidental unless careful search has excluded a carcinomatous change in the periphery of the scarred lungs.

Adenocarcinoma↗
PubMed2005

[Effects of moxibustion at Feishu (BL 13) and Gaohuang (BL 43) on expression of TGF-beta1 in the bleomycin -induced pulmonary fibrosis].

OBJECTIVE: To explore the mechanism of moxibustion arresting the pulmonary fibrosis and provide experimental basis for prevention and treatment of pulmonary fibrosis with acupuncture and moxibustion. METHODS: One hundred and forty SD rats were randomly assigned to 4 groups: a blank group, a model group, a moxibustion group and a prednisone group, 35 rats in each group. The 3 groups expect the blank group were injected with bleomycin via trachea to induce experimental pulmonary fibrosis model, and 7 days after modeling, they were treated with moxibustion at bilateral Feishu (BL 13) and Gaohuang (BL 43), 3 cones each point, once each day, 10 days constituting one therapeutic course with an interval of one day between courses. After 3 courses, all rats were killed and expressions of TGF-beta1mRNA were detected with PCR method. RESULTS: The content of TGF-beta1mRNA in the pulmonary tissue in the moxibustion group and the prednisone group was significantly lower than the model group (P < 0.01), and there was no significant difference between the moxibustion group and the prednisone group (P > 0. 05). CONCLUSION: Both moxibustion at Feishu (BL 13) and Gaohuang (BL 43), and prednisone treatment can significantly suppress the expression of TGF-beta1mRNA in the pulmonary tissue in the rat of bleomycin-induced pulmonary fibrosis.

Animals↗
PubMed1989

[Pulmonary fibrosis and antioxidant agents].

Lung inflammatory cells in idiopathic pulmonary fibrosis (IPF) is characterized by an increased spontaneous production of oxidants. This suggests that the oxidants may play a role in causing the epithelial cell injury in the early stage of IPF. Bleomycin (BLM) induces pulmonary fibrosis by oxidant production. We tested the hypothesis that a dietary supplement of vitamin E (VE) may protect against, and its deficiency may exacerbate, BLM-induced pulmonary fibrosis. Because the hamster is known to be the best model among animals studied mimicking human lung antioxidant enzyme activities, Syrian Golden hamsters were used in this study. In dietary VE supplement and BLM treated group (Ead.B), mean serum VE concentration increased by about 3 times that of control (C) and the BLM treated group (CB). Despite the remarkably high VE content, no significant difference was found between CB and Ead.B for pressure-volume (PV) curves and morphological data. In BLM treated with dietary VE deficient group (Ede.B), serum VE concentrations markedly decreased on all experimental days compared with other groups. Mechanical properties in P-V curves of Ede.B showed most less distensible characteristics in early stage and most distensible characteristics in later stage. These emphysematous changes observed in P-V curves in the later stage of Ede.B, coincided with the morphological observations. In the early stage of BLM treatment, lipid peroxide concentrations in the lung tissue were significantly higher in Ede.B compared with other groups. It was concluded that a dietary supplement of VE cannot protect against BLM-induced pulmonary fibrosis, and a dietary VE deficiency exacerbates BLM lung injury to produce on emphysema in the hamster.

Animals↗
PubMed2002

Surfactant protein-A in lung lavage fluid obtained from patients with idiopathic pulmonary fibrosis.

BACKGROUND: Alterations in surface-active material may contribute to the pathogenesis of idiopathic pulmonary fibrosis both by increasing the elastic recoil due to surface forces and by promoting alveolar collapse. This study intends to evaluate the surfactant protein-A levels in bronchoalveolar lavage in patients of idiopathic pulmonary fibrosis. MATERIAL AND METHODS: Ten patients of idiopathic pulmonary fibrosis (IPF) of either sex were taken up for estimation of surfactant protein-A (SP-A) levels in bronchoalveolar lavage. The final diagnosis of IPF was based on histopathology and high resolution CT. Ten controls were taken out of which five patients were histopathologically proven cases of sarcoidosis and five patients with normal chest X-ray and CT scan. History, physical examination and routine investigations were done to rule out any concomitant illness. RESULTS: Age range of patients varied from 37-65 years (mean +/- SD of 50.65 +/- 9.05) and controls 30-62 years (42.50 +/- 9.95). Fiberoptic bronchoscopy and bronchoalveolar lavage was carried out and fluid aspirated was studied for surfactant protein-A. The level of surfactant protein-A recovered was lower in patients with idiopathic pulmonary fibrosis in comparison to control group p < 0.01 (1.86 +/- 1.26 and 5.76 +/- 2.0 microg/ml respectively). The levels of surfactant protein-A also revealed that the level decreased with derangement of pulmonary function. CONCLUSIONS: The study thus showed that the level of surfactant protein A is reduced in patients with idiopathic pulmonary fibrosis. It is likely that they have a significant role in pathogenesis of idiopathic pulmonary fibrosis and its progression. Surfactant-A may have important therapeutic implications. Further studies are required for a definite answer.

Adult↗
PubMed1992

Neutrophilic alveolitis in idiopathic pulmonary fibrosis. The role of interleukin-8.

Idiopathic pulmonary fibrosis is an immunologically mediated pulmonary disorder in which activated alveolar macrophages (AM) and neutrophils play cardinal roles in the pathogenesis of the inflammatory lung lesion. The factors responsible for the induction and perpetuation of the neutrophilic alveolitis are not known. Recently, a novel cytokine (Interleukin-8) was described that is released by activated mononuclear phagocytes and a variety of other cell types, and it exhibits potent chemotactic activity for polymorphonuclear leukocytes (PMN). Increased expression of IL-8 has been described in other inflammatory disorders characterized by neutrophilic infiltration, including psoriasis, rheumatoid arthritis, and the sepsis syndrome, but no studies have assessed this cytokine in the context of interstitial pulmonary disorders. We have previously shown that normal human AM release IL-8 upon appropriate stimulation, but data assessing the expression of IL-8 by human AM in specific pulmonary disease states are lacking. In this study, we examined the expression of steady-state mRNA for IL-8 by human alveolar macrophages obtained by bronchoalveolar lavage (BAL) from patients with idiopathic pulmonary fibrosis (IPF) or sarcoidosis and from healthy volunteers. Because it is known that adherence to plastic culture plates may up-regulate gene expression for IL-8 in the absence of additional stimulation, we extracted mRNA immediately from the cell pellet obtained by BAL rather than using cultured alveolar macrophage monolayers. Northern blot analysis was performed to determine IL-8 mRNA expression. We found that BAL cells from patients with IPF constitutively expressed mRNA for IL-8, and the amount of IL-8 mRNA (as assessed by laser densitometry) correlated with the percent of neutrophils on BAL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Interstitial pulmonary fibrosis in an automobile body shop worker.

Interstitial pulmonary fibrosis (IPF) is often of uncertain etiology and is therefore named 'idiopathic' pulmonary fibrosis. Some occupational exposures, however, are known to cause interstitial fibrosis, asbestos and silica being well-known examples. We present clinical and pathological findings of a case with IPF and the results of microchemical analysis of inorganic particulate matter in the lung tissue. A very high lung burden of inorganic contaminants was found, including silica and metallic compounds. Emphasis is given to the importance of obtaining detailed occupational histories and conducting microchemical analysis of lung tissue in order to clarify etiological factors in cases with 'idiopathic' pulmonary fibrosis.

Aged↗
PubMed1997

Effects of neutrophil elastase inhibitor on bleomycin-induced pulmonary fibrosis in mice.

Neutrophils play an important role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). To elucidate the possible involvement of neutrophil elastase (NE) in pulmonary fibrosis, we investigated the efficacy of a new specific NE inhibitor (ONO-5046 Na) in a murine model of human IPF, bleomycin-induced pulmonary fibrosis. Bronchoalveolar lavage (BAL) and histopathological analysis were performed on bleomycin-treated mice (group A), bleomycin and ONO-5046 Na-treated mice (group B), and saline control groups at 1, 15, and 29 d after the end of bleomycin treatment. At 29 d, multifocal fibrosis was observed in group A, whereas no fibrotic regions were observed in group B. Interleukin-1 beta and macrophage inflammatory protein-2 mRNA levels in BAL cells on day 1, and platelet-derived growth factor-A and insulin-like growth factor-1 mRNA levels on days 1 and 15, were significantly lower in group B than in group A. Thus, we demonstrated an inhibitory effect of ONO-5046. Na on pulmonary fibrosis in mice, indicating the involvement of NE in the pathogenesis of pulmonary fibrosis. We propose that this effect might be related to suppressed expression of particular cytokines in alveolar macrophages and that this specific NE inhibitor could be a novel therapeutic agent for IPF.

Animals↗